Navegando por Autor "Silva, João Santana da"

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Diet rich in lard promotes a metabolic environment favorable to Trypanosoma cruzi growth.
(2021) Souza, Débora Maria Soares de; Silva, Maria Cláudia; Farias, Sílvia Elvira Barros; Menezes, Ana Paula de Jesus; Milanezi, Cristiane Maria; Lúcio, Karine de Pádua; Paiva, Nívia Carolina Nogueira de; Vieira, Paula Melo de Abreu; Costa, Daniela Caldeira; Pinto, Kelerson Mauro de Castro; Costa, Guilherme de Paula; Silva, João Santana da; Silva, André Talvani Pedrosa da
Background: Trypanosoma cruzi is a protozoan parasite that causes Chagas disease and affects 6–7 million people mainly in Latin America and worldwide. Here, we investigated the effects of hyperlipidic diets, mainly composed of olive oil or lard on experimental T. cruzi infection. C57BL/6 mice were fed two different dietary types in which the main sources of fatty acids were either monounsaturated (olive oil diet) or saturated (lard diet). Methods: After 60 days on the diet, mice were infected with 50 trypomastigote forms of T. cruzi Colombian strain. We evaluated the systemic and tissue parasitism, tissue inflammation, and the redox status of mice after 30 days of infection. Results: Lipid levels in the liver of mice fed with the lard diet increased compared with that of the mice fed with olive oil or normolipidic diets. The lard diet group presented with an increased parasitic load in the heart and adipose tissues following infection as well as an increased expression of Tlr2 and Tlr9 in the heart. However, no changes were seen in the survival rates across the dietary groups. Infected mice receiving all diets presented comparable levels of recruited inflammatory cells at 30 days post-infection but, at this time, we observed lard diet inducing an overproduction of CCL2 in the cardiac tissue and its inhibition in the adipose tissue. T. cruzi infection altered liver antioxidant levels in mice, with the lard diet group demonstrating decreased catalase (CAT) activity compared with that of other dietary groups. Conclusions: Our data demonstrated that T. cruzi growth is more favorable on tissue of mice subjected to the lard diet. Our findings supported our hypothesis of a relationship between the source of dietary lipids and parasite-induced immunopathology.
Increased type 1 chemokine expression in experimental Chagas disease correlates with cardiac pathology in Beagle dogs.
(2010) Guedes, Paulo Marcos da Matta; Veloso, Vanja Maria; Silva, André Talvani Pedrosa da; Diniz, Lívia de Figueiredo; Caldas, Ivo Santana; Matta, Maria Adelaide do Valle; Silva, Juliana Santiago; Chiari, Egler; Galvão, Lúcia Maria da Cunha; Silva, João Santana da; Bahia, Maria Terezinha
Chemokines and chemokine receptors interaction have presented important role in leukocyte migration to specific immune reaction sites. Recently, it has been reported that chemokine receptors CXC (CXCR3) and CC (CCR5) were preferentially expressed on Th1 cells while CCR3 and CCR4 were preferentially expressed on Th2 cells. This study evaluated the mRNA expression of type 1 and type 2 chemokine and chemokine receptors in the cardiac tissue of Beagle dogs infected with distinct genetic groups of Trypanosoma cruzi (Y, Berenice- 78 and ABC strains) during acute and chronic phases. To analyze the correlation between chemokine and chemokine receptors expression and the development of heart pathology, the chronic infected animals were divided into groups, according to the parasite strain and based on the degree of heart damage: cardiac and indeterminate form of Chagas disease. Our results indicated that cardiac type1/2 chemokines and their receptors were partially dependent on the genetic diversity of parasites as well as the polarization of clinical forms. Also, dogs presenting cardiac form showed lower heart tissue mRNA expression of CCL24 (type 2) and higher expression of CCL5, CCL4 and CXCR3 (type 1) when compared with those with indeterminate form of disease. Together, these data reinforce a close-relation between T. cruzi genetic population and the host specific type 1 immune response and, for the first time, we show the distribution of type 1/2 chemokines associated with the development of cardiac pathology using dogs, a well similar model to study human Chagas disease.
Interferon-y-induced nitric oxide causes intrinsic intestinal denervation in Trypanosoma cruzi-infected mice.
(2004) Arantes, Rosa Maria Esteves; Marche, Homero H. F.; Bahia, Maria Terezinha; Cunha, Fernando de Queiroz; Rossi, Marcos Antonio; Silva, João Santana da
In this study, the role of nitric oxide (NO) in neuronal destruction during acute-phase Trypanosoma cruzi infection was evaluated in male C57BL/6 (WT, wildtype) mice and knockout mice [inducible nitric oxide synthase (iNOS)_/_ and interferon (IFN)_/_]. Selected animals were infected by intraperitoneal injection of 100 trypomastigote forms of the Y strain of T. cruzi. Others were injected intraperitoneally with an equal volume of saline solution and served as controls. Our findings support those of previous studies regarding myenteric denervation in acute-phase T. cruzi infection. In addition, we clearly demonstrate that, despite the fact that parasite nests and similar inflammatory infiltrate in the intestinal wall were more pronounced in infected iNOS_/_ mice than in infected WT mice, the former presented no reduction in myenteric plexus neuron numbers. Neuronal nerve profile expression, as revealed by the general nerve marker PGP 9.5, was preserved in all knockout animals. Infected IFN_/_ mice suffered no significant neuronal loss and there was no inflammatory infiltrate in the intestinal wall. On days 5 and 10 after infection, iNOS activity was greater in infected WT mice than in controls, whereas iNOS activity in infected knockout mice remained unchanged. These findings clearly demonstrate that neuronal damage does not occur in NO-impaired infected knockout mice, regardless of whether inflammatory infiltrate is present (iNOS_/_) or absent (IFN_/_). In conclusion, our observations strongly indicate that myenteric denervation in acutephase T. cruzi infection is because of IFN-_-elicited NO production resulting from iNOS activation in the inflammatory foci along the intestinal wall.